Post-Translational Modification of NaV1.8 Peptide Alters Analgesic Efficacy in Acute and Chronic Pain Models

Abdulelah Ahmed and Kwaku Bonsu

Post Successful Surgery Picture.

A picture taken after a successful surgery.

Undergraduate Student Project


Did you know that pain is the most common reason people seek out medical care? Yet, available treatments have limited effectiveness for a majority of people. My name is Abdulelah Ahmed. I am a junior Biomedical Sciences major at the University at Buffalo. With the generous support of the UB Collegiate Science and Technology Entry Program (CSTEP), I participated in their intensive summer research program, where I conducted research under Dr. Arin Bhattacharjee as my mentor. Dr. Bhattacharjee's lab is interested in identifying novel targets to treat acute and chronic pain, specifically focusing on ion channel trafficking mechanisms. My job is to use pharmacological tools developed in the lab to test analgesic efficacy in rodent pain models. I am also conducting animal surgeries that mimic clinical post-operative pain and performing behavioral experiments. While there are helpful treatments for inflammatory pain, such as opioids, adverse side effects associated with these drugs limit their long-term use and compromise patient compliance. Given the national opioid crisis, many in the medical community have significantly reduced their prescriptions. Chronic pain is one of the most debilitating diseases in the United States and a public health concern. With that comes the great need for good alternatives to treat post-surgical and chronic pain.


Nociceptive dorsal root ganglion (DRG) neurons remain central sites for investigative study as neuronal plasticity underlies pain states. During tissue damage, inflammatory mediators initiate signal transduction in DRG neurons-altering channel properties and accompanying pain perception. Chronic exposure to inflammatory mediators leads to hyperplasia, allodynia, and spontaneous pain. Voltage-dependent sodium (NaV) 1.8 channels regulate action potential generation in nociceptive neurons, identifying them as putative analgesic targets. Previously, we have found that dorsal root ganglion (DRG)-specific knockdown of Magi-1 attenuated thermal nociception and acute inflammatory pain and produced deficits in NaV1.8 protein expression. A competing cell-penetrating peptide mimetic derived from the NaV1.8 WW binding motif known as PY (proline tyrosine motif) peptide,  decreased sodium currents, reduced NaV1.8 protein expression, and produced hypo-excitability. Using rodent models, genetic and pharmacological tools, we have demonstrated that Magi-1 significantly reduced pain behaviors in acute and chronic inflammatory pain for a prolonged period of time.

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